Chagas disease frequently causes megacolon. We investigated the enteric nervous systems in patients with chagasic megacolon compared to idiopathic megacolon and controls. Surgical specimens were obtained from 12 patients with chagasic megacolon (1 woman, 11 men, age range 41 to 72 y) and 9 patients with idiopathic megacolon (3 women, 6 men, age range 39 to 68 y), undergoing surgery for intractable constipation. A control group of 10 patients (9 women, 1 man, age range 43 to 75 y) undergoing left hemicolectomy for nonobstructing colorectal cancer was also studied. Colonic sections were investigated by conventional and immunohistochemical methods, also taking into consideration the presence of lymphocytes. Compared to controls, the 2 megacolon groups showed a decrease of enteric neurons (not due to increased apoptosis) and of enteric glial cells (all more important in chagasic patients). The interstitial cells of Cajal subtypes were decreased but not absent in megacolons, although an increase of the intramuscular subtype was found, suggesting a possible compensative mechanism. An increased amount of fibrosis was found in the smooth muscle and the myenteric plexus of chagasic patients compared to the idiopathic megacolon and the control group. A mild lymphocytic infiltration of the enteric plexuses (more evident in Chagas disease) was also found in megacolons but not in controls. Patients with chagasic megacolon display important abnormalities of several components of the enteric nervous system. Similar alterations, although of lesser severity, may be found in patients with idiopathic megacolon.

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Chagas' disease and idiopathic achalasia have similar esophageal manifestations such as absent or incomplete lower esophageal sphincter relaxation and aperistalsis in the esophageal body (alterations seen mainly in the distal esophageal body). Our aim in this paper was to study the response of the proximal esophageal body to wet swallows in patients with Chagas' disease and patients with idiopathic achalasia. We retrospectively analyzed the time interval between the onset of the pharyngeal contractions 1 cm proximal to the upper esophageal sphincter, as well as 5 cm distal to the pharyngeal measurement. Amplitude, duration and area under the curve of contractions in the proximal esophagus were also determined in 42 patients with Chagas' disease (15 with associated esophageal dilatation), 21 patients with idiopathic achalasia (14 with concomitant esophageal dilatation) and 31 control subjects. The time between the onset of pharyngeal and proximal esophageal contractions was longer in patients with Chagas' disease and in those with esophageal dilatation (1.39 +/- 0.16 s) than in control subjects (0.86 +/- 0.04 s, P < 0.01). The amplitude of proximal esophageal contractions was lower in patients with idiopathic achalasia and esophageal dilatation (60.9 +/- 16.3 mmHg) than in control subjects (89.7 +/- 6.9 mmHg, P = 0.06). The authors conclude that in patients with advanced esophageal disease, the proximal esophageal contractions in Chagas' disease have a delayed response to wet swallows when compared with controls, and that the amplitude of proximal esophageal contractions was lower than expected in patients with idiopathic achalasia.

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